Transcript Management of the Stridulous Child

Stridor in Child
Definitions
 Stridor
 Harsh sound
produced by turbulent
airflow through a
partial obstruction
 May be soft and
tuneful/musical quality
 Characteristic of
certain pathology but
never diagnostic
 Stertor
 Snoring type of noise
often made by
nasopharyngeal or
oropharyngeal
obstruction
 May occassionally be
created by
supraglottic larynx
Pathophysiology of Stridor
 Based on Venturi
principle
 When a gas passes
through a narrowed
tube/trachea, the
lateral pressure that
has held the lumen
open can drop very
quickly causing the
tube/lumen to close.
Venturi Vuneralbility
(Pathophys cont’d)
 Pediatric airway more flexible
 Forces exerted by Venturi principle cause
the narrowed, flexible airway to be
momentarily closed during either
inspiration or expiration.
 Pattern of intermittent flow creates pattern of
vibrations yielding audible sounds
Anatomy
 Infant larynx situated high in the neck
with epiglottis located behind soft palate.
 Pharyngeal structures in closer proximity
compared to adult
 Hyoid bone higher
Anatomy
 Anatomic differences associated with
infant airway create a separation
between airway and digestive tract.
 Air movement is predominantly
transnasal
 As child grows, larynx descends
 Larger pharynx to facilitate speech
production
 Common conduit for food and air passage
 Increases risk for foreign bodies, food, gastric
contents to enter airway
Evaluation
 History
 Helpful pneumonic:
SPECS-R
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Severity
Progression
Eating difficulties
Cyanosis
Sleep disturbance
Radiologic findings
*Don’t forget to inquire about
birth history, maternal STD,
history of intubation
Physical Assessment
First Things First
 Assess severity/need
for emergent airway
(ABC’s)
 Noninvasive
inspection
 Indicators of severity
 Respiratory rate
 Level of
conciousness/mental
status
 Accessory muscle use
 Signifies significant
obstruction
 Auscultation
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Lung fields
Neck
Mouth
Nose
Further Assessment
 If child d/n have impending respiratory
failure, a more detailed physical exam
should be performed
 General (weight, growth percentile,
development)
 Nasal cavity, oral cavity and oropharynx
more thoroughly examined
 Flexible fiberoptic laryngoscopy
Endoscopy
 In unusual/difficult cases
to determine etiology of
stridor.
 Laryngoscope, Hopkins
rod-lens telescopes,
bronchoscope
 Verify all equipment/light
sources work!
 Trach tray in room just in
case.
 Good communication
btwn endoscopist and
anesthesiologist is a
must.
Outline
I.
II.
III.
IV.
V.
VI.
Nose &
Nasopharynx
Oropharynx or
hypopharynx
Supraglottic larynx
Glottic larynx
Subglottic larynx
Tracheobronchial
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Congenital
Infectious
Traumatic
Neoplastic
Vascular
Iatrogenic
Toxic/metabolic
Choanal Atresia (CA)
 Epidemiology
 Rare: 1 in 10,000 births
 Females >males
 50% unilateral, 50% bilateral
 2 types: membranous or bony
 29% bony
 71% mixed bony-membranous (Brown et al,
Laryngoscope 1996)
 Pathogenesis controversal
Choanal Atresia (CA)
 Clinical signs & sx
 Respiratory
distress/paradoxical
cyanosis
 Feeding difficulty
 Associated abnormalities
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C- Coloboma
H- Heart anomaly
A- Atresia of choana
R- Retarded growth
G- Genital hypoplasia
E- Ear anomalies and/or
deafness
 Clues to diagnosis
 Inability to pass 8 Fr
catheter beyond 3.5 cm
from nasal vestibule
 Flexible scope hits a “brick
wall” during exam
 Mirror under nares fails to
fog on expiration
 Axial CT confirms
diagnosis
Choanal Atresia
 Management
 InitialMcGovern nipple
 Oral airway or McGovern nipple
 Surgical
 Transpalatal
 Better visualization, high success rate
 Can damage palate growth plate=cross bite deformities
 Transnasal
 Less blood loss, faster procedure
 Increased CSF leak and meningitis risk
 Laser
 CO2, KTP, Holmium:YAG
 Good success with KTP + endoscopic techniques
 Operating microscope with CO2 laser also being employed
Laryngomalacia
 General
 Most common cause of congenital stridor
 May manifest days/weeks after birth
 Symptoms usually resolve by 12-18months
 Pathophysiology
 Stridor caused by prolapse of supraglottic
structures into laryngeal inlet
Laryngomalacia
 Signs/Symptoms
 low, pitched fluttering inspiratory stridor
 Peaks at 6-9months
 Positional variations
 Exacerbated by activity (i.e. feeding, exertion)
 Rarely produces cyanosis
 Cyanosis should prompt suspicion for other
pathology
Laryngomalacia
Laryngomalacia
 Physical exam
 Fiberoptic
laryngoscopy while
child is awake
 Direct
laryngoscopy/broncho
-scopy sometimes
needed to rule out
synchronous lesions
Laryngomalacia
 Management
 Self-limited condition; majority of cases
resolve
 Surgical treatment (~10% of cases)
 Supraglottoplasty
 Indicated for cases with severe stridor, failure to thrive,
apneas, cor pulmonale, pulmonary HTN
Congenital Laryngeal Web
 Pathogenesis
 Arise from failure of recanalization of larynx in
embryo
 Location
 Predominantly in the anterior glottis
 Associated findings
 Severe webbing assoc. with subglottic stenosis.
 Laryngeal atresia requires trach at birth
 Anterior glottic webs assoc. w/ velocardiofacial
syndrome (22q11 deletion) (Oto Head & Neck 2004 130: 415-17)
 Symptoms
 Present with abnormal cry, stridor
Congenital Laryngeal Web
 Diagnostic endoscopy
 Required for diagnosis
 Other abnormalities must be ruled out as
well
 Treatment
 Simple insicion for small webs
 Laryngofissure with stenting for severe
webbing.
 Endoscopic laser treatment also an option
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Vocal Cord Paralysis
 General
 10% of congenital
laryngeal lesions
 May be congenital or
acquired
 Most often cause is
idiopathic
 Etiologies
 Traumatic/Iatrogenic
 Obstetric/birth trauma
 Cardiac surgery
 Esophageal surgery
 Other congenital
abnormalities
 Cardiac anomalies
 CNS origin
 Chiari malformation
Chiari malformation
Vocal Cord Paralysis
 Unilateral
 Breathy voice/cry
 Mild stridor and/or
dyspnea
 Aspiration
 Treatment
 Speech therapy
 If tracheotomy needed,
decannulation is
usually possible as
child/larynx developes
 Bilateral
 Severe stridor
 Aspiration
 Treatment
 tracheotomy usually
required
 Serial endoscopies
 Surgery after at least 1
year after trach w/o
improvement
Vocal Cord Paralysis
 Evaluation
 Can be seen with FOL while pt is awake
 Laryngotracheobronchoscopy must be performed
 Must palpate arytenoids
 Exclude synchronous lesions
 MRI brain, brain stem, neck and chest reasonable if
cause not obvious (course of vagus)
 FEES/MBS may be utilized in cases of aspiration
 Management
 VFP in infants usually resolves in 6-18mos
 Scheduled monitoring is reasonable for first 2 yrs
 Temporary tracheotomy may be necessary
Vocal Cord Paralysis
 Surgical methods
 CO2 transverse partial cordotomy
 Costal cartilage grafting
 Arytenoidopexy w/wo arytenoidectomy
 CO2 laser
 External approach
Subglottic Stenosis
 Congenital
 Dx made in absence
of factors causing
acquired stenosis
 Moderate-severe
stenosis=Stridor at
birth.
 Mild stenosis=
Intermittent stridor
 Acquired
 More common than
congenital
 Usually more severe
and difficult to
manage
 Endotracheal
intubation
trauma=most
commom cause
Subglottic Stenosis
 Clinical signs/symptoms
 Degree of stenosis dictates symptoms
 Severe stenosis, infant may have stridor at birth
 Mild stenosis may not manifest until URI takes
place.
 In acquired SGS, a clue in neonates may be
failed extubation trial.
 Older children may successfully extubate but
present later with progressive worsening
respiratory distress
Subglottic Stenosis
 Evaluation
 Stenosis may be visualized on plain films
 Direct laryngoscopy/tracheoscopy needed
for confirmation and airway may be staged
at this point.
 Prevention
 Use of uncuffed, polyvinylchloride ETT
 Smaller tubes
 Nasotracheal intubation
Subglottic Stenosis
 Treatment options
 Primary goal is to
achieve
decannulation (if
tracheostomy present)
or prevent
tracheostomy
 Conservative
 Observation (grades III)
 Temporizing measure
 Tracheostomy
 Definitive Surgical
Options
 Endoscopic methods
 Laser
 Anterior cricoid split
 Laryngotracheal
reconstruction
 Cricotracheal
resection
Tracheomalacia
 Congenital deformity of tracheal rings
 Expiratory stridor/respiratory distress
 Depends on extent of lesion
 Diagnosis
 Flexible bronchoscopy with awake patient
 Collapse of anterior tracheal wall against membranous
posterior portion
 Treatment rarely needed as most cases are
self limited
 Some cases may need temporary tracheotomy
 In secondary tracheomalacia, treatment directed at
underlying cause.